Renal amyloidosis in a family of beagles.

Renal amyloidosis was confirmed in 6 related male and female Beagles, ranging in age from 5 to 11 years. The most commonly reported signs of illness included lethargy, anorexia, vomiting, and weight loss. Common clinicopathologic abnormalities were normocytic, normochromic anemia; hypoalbuminemia; azotemia; hypercholesterolemia; proteinuria; and urine specific gravity values below the normal range. Histologic examination of renal tissue from the 6 Beagles revealed moderate to severe glomerular amyloidosis with inconsistently observed mild medullary interstitial amyloidosis. Congo red-stained kidney sections from 4 of 4 affected dogs were potassium permanganate-sensitive, suggestive of reactive amyloidosis. Hereditary predisposition for renal amyloidosis was suspected in these Beagles.     

Familial renal amyloidosis in Chinese Shar Pei dogs

Renal amyloidosis was diagnosed in 14 young Chinese Shar Pei dogs, all of which were related. Clinical signs were those of renal failure and included vomiting, anorexia, lethargy, polydipsia, polyuria, weight loss, and dehydration. Some dogs had a history of intermittent fever and joint swelling. Laboratory findings also were compatible with renal failure and included azotemia, hyperphosphatemia, low total CO2 content in serum, isosthenuria, proteinuria, and hypercholesterolemia. All dogs had medullary deposition of amyloid, and 9 of 14 (64%) had glomerular involvement. The remaining renal lesions were typical of end-stage renal disease. In some dogs, amyloid deposits were found in other tissues (eg, liver, spleen, stomach, small intestine, myocardium, lymph node, prostate gland, thyroid gland, and pancreas). Amyloid deposits were sensitive to potassium permanganate oxidation, suggesting the presence of amyloid protein AA.     

Senile cardiac amyloidosis in the dog

Thirty-two cases of senile cardiac amyloidosis from a routine necropsy material of 594 dogs were studied. The age of the affected dogs ranged from 10 to 16 years. Amyloid was observed in the intramural arteries and arterioles, predominantly in the ventricular myocardium. The vessels were often obturated with amyloid, and myocardial necroses and fibroses were common consequences of the vascular lesions. In three cases amyloid deposits were also observed in the main subepicardial coronary arteries. In contrast to man, only slight interstitial amyloid degeneration was found in four of the dogs observed. Amyloid in the mitral valves, tricuspid valves and aortic cusps was observed in six, two and three cases respectively. It was concluded that the distribution of senile cardiac amyloidosis in the heart of the dog differs considerably from that in man.     

Progressive renal disease in Soft-coated Wheaten Terriers: possible familial nephropathy

Clinical and pathological features are described in seven young Soft-coated Wheaten Terriers with chronic renal disease. The oldest dog was 21/2 years; in the other six, ages at death ranged from one to 15 months. Two of the puppies were littermates: one died at 4 weeks, the other at 12 months. Two of the dogs were examined at intervals up to 14 months, during which time there was progressive deterioration in renal function. All seven dogs had abnormal kidneys with cortical narrowing. The histological features were not consistent and included: tubular dilatation and basement membrane thickening; an unusually large proportion of immature glomeruli; persistence of interstitial connective tissue resembling foetal mesenchyme. Inflammatory change was minimal except in two dogs with super-imposed pyelonephritis. The clinical and laboratory data suggest that these dogs had dysplasia of the kidneys that progressed to chronic renal disease during early life. In three dogs there was a familial relationship.     

Renal medullary amyloidosis in Dorcas gazelles

Between January 1976 and September 1987 renal medullary amyloidosis (RMA) was diagnosed in 17 Dorcas gazelles; the necropsy prevalence rate was 17/32 (53%). The most severe amyloid deposits were in the renal medulla; glomeruli were spared. Renal cortical lesions of interstitial fibrosis and tubular atrophy and dilatation significantly correlated with RMA (P less than 0.01) and were considered to be secondary changes. There were varying degrees of lymphoplasmacytic inflammation and tubular cast formation which did not significantly correlate with RMA. Amyloid was confirmed histochemically and by electron microscopy and was identified as AA type by the permanganate method. Progressive renal failure was the cause of death or necessitated euthanasia in 7/17 (41%) gazelles. RMA in Dorcas gazelles does not appear to be familial. A high prevalence of chronic or recurring Actinomyces (Corynebacterium) pyogenes infections may be an important factor.     

Comparative aspects and clinical outcomes of canine renal hemangiosarcoma

BACKGROUND: Hemangiosarcoma (HSA) is a common solid tumor of the spleen, heart, and skin of dogs. Renal HSA represents an uncommon anatomic variant, with little reported about its biologic behavior and clinical outcome. HYPOTHESIS: That renal HSA is associated with longer survival than other visceral forms of HSA. ANIMALS: 14 dogs with renal HSA. METHODS: Medical records from 1999 to 2004 were searched for dogs with histopathologically confirmed renal HSA, and data relevant to clinical signs, treatments, and outcomes were abstracted. RESULTS: Clinical signs were nonspecific, and the median duration of clinical signs before diagnosis was 60 days. Two dogs presented in cardiovascular collapse secondary to hemoperitoneum. Common hematologic and biochemical abnormalities were anemia (9/14), hematuria (7/14), and proteinuria (7/14). One dog had pulmonary metastasis at diagnosis. All dogs had evidence of a renal mass visualized by abdominal radiography (14/14), ultrasound (9/14), or both. All dogs underwent nephrectomy, and 4/14 dogs also received adjunctive chemotherapy. Median survival time of all dogs was 278 days (range 0-1,005 days), and dogs with hemoperitoneum had significantly shorter survival times than dogs without hemoperitoneum (62 days versus 286 days, P < .001). CONCLUSIONS AND CLINICAL IMPORTANCE: These results indicate that hemoperitoneum and distant metastasis at diagnosis appear to occur less frequently in dogs with renal HSA compared with other visceral forms of HSA. Furthermore, dogs with renal HSA have protracted disease progression, with improved 1-year survival rates and longer median survival time compared to dogs with splenic, cardiac, and retroperitoneal HSA.     

Chronic renal failure in young dogs–possible renal dysplasia

The clinico-pathological findings are described in thirteen young dogs with advanced renal disease. All but three dogs were less than 2 years old. Some had signs of renal dysfunction since birth. Presenting signs were variable but anorexia, lethargy and weight loss were most frequent. All dogs had raised blood urea levels and most passed dilute urine; proteinuria and anaemia were variable findings. At necropsy all dogs had extra-renal lesions of renal failure and finely granular or lobulated, shrunken kidneys. The microscopical appearances of the kidneys were not those of amyloidosis, inflammatory or glomerular disease but were considered likely to be of developmental origin. The renal lesions were divided into three histologically distinct groups.

• 1 Predominantly cystic and connective tissue changes, characterized by striking dilatation of glomerular capsular spaces and cortical tubules.
• 2 Atypical connective tissue changes in which there were segmental bands of fibrous tissue containing primitive glomerular and tubular structures.
• 3 Predominantly glomerular and connective tissue changes, characterized by varying degrees of glomerulosclerosis and widespread calcification of glomeruli, tubules and blood vessels.

All groups had cortical and medullary interstitial fibrosis but minimal inflammatory cell infiltrates.     

Concurrent renal amyloidosis and thymoma resulting in a fatal ventricular thrombus in a dog

Thymoma‐associated nephropathies have been reported in people but not in dogs. In this report, we describe a dog with thymoma and concurrent renal amyloidosis. A 7‐year‐old castrated male Weimaraner was presented for progressive anorexia, lethargy, and tachypnea. The dog was diagnosed with azotemia, marked proteinuria, and a thymoma that was surgically removed. Postoperatively, the dog developed a large left ventricular thrombus and was euthanized. Necropsy confirmed the presence of a left ventricular thrombus and histopathology revealed renal amyloidosis. We speculate that the renal amyloidosis occurred secondary to the thymoma, with amyloidosis in turn leading to nephrotic syndrome, hypercoagulability, and ventricular thrombosis. This case illustrates the potential for thymoma‐associated nephropathies to occur in dogs and that dogs suspected to have thymoma should have a urinalysis and urine protein creatinine ratio performed as part of the pre‐surgical database.     

Suspected familial renal disease in chow chows

Renal disease was diagnosed in 6 young Chow Chows. Clinical abnormalities included vomiting, polyuria, polydipsia, and weight loss. Common abnormal laboratory findings were azotemia, hyperphosphatemia, hypocalcemia, nonregenerative anemia, and low urine specific gravity. All 6 dogs had similar microscopic renal lesions. characterized by interstitial fibrosis, a population of small glomeruli, and lack of inflammatory cells. A familial basis for the renal disease is suggested because of its development in 4 closely related dogs.     

Glomerular deposition of immune complexes in dogs following natural infection with canine adenovirus.

The renal lesions were studied in eight dogs which had either died as a result of acute canine adenovirus infection (Rubarth's disease) or were in various stages of recovery from the clinical disease. Using immunofluorescence techniques granular deposits of IgG were detected in the glomeruli of six dogs; four of these animals had similar glomerular deposits of canine adenovirus antigen. Eluates obtained from kidney tissue of four dogs were found to contain antiviral antibody. Histologically those animals in which glomerular deposits of IgG and viral antigen were detected showed segmental glomerular hypercellularity. These findings were attributed to the deposition of circulating virus antigen-antibody complexes in the glomeruli.     

Results of surgical treatment for hyperadrenocorticism caused by adrenocortical neoplasia in the dog: 25 cases (1980-1984)

Results of surgical treatment for neoplasia of the adrenal cortex that caused hyperadrenocorticism were evaluated in 25 dogs. Surgical examination of the adrenal glands was performed by use of a ventral midline approach in 24 dogs and a retroperitoneal approach in 1 dog. All 25 dogs had a unilateral, adrenocortical tumor. Histologic examination identified 14 adrenocortical carcinomas and 11 adenomas. Seven dogs with carcinoma had visible metastasis to the liver, 3 had local invasion into the caudal vena cava, and 1 had extension into the adjacent renal vein. Seven of the 9 dogs with metastasis were euthanatized at time of surgery. Of the remaining 18 dogs that survived surgery, 9 (4 with carcinoma and 5 with adenoma) developed serious postoperative complications including acute renal failure, pneumonia, and pulmonary artery thromboembolism; 8 of these dogs died or were euthanatized. Of the remaining 10 dogs, clinical signs associated with hyperadrenocorticism resolved in the 7 dogs that had adrenocortical adenoma and in 1 of the 3 dogs that had carcinoma. The remaining 2 dogs with carcinoma had persistent hyperadrenocorticism and were treated with high doses of mitotane. Although no response was observed in 1 dog with visible hepatic metastasis, a decrease in serum cortisol concentrations and resolution of clinical signs were detected in the other dog during prolonged daily administration of mitotane.     

Juvenile nephropathy in 37 boxer dogs

OBJECTIVES: The purpose of this study was to review and characterise the clinical presentation of young boxer dogs with chronic kidney disease referred to the authors' institutions. METHODS: Records were collected retrospectively from 37 boxer dogs, less than five years of age, which had presented with azotaemia, inappropriately low urine concentrating ability, and ultrasound or radiographic evidence of abnormal kidneys. RESULTS: Clinicopathological findings included azotaemia, hyperphosphataemia, anaemia, isosthenuria and proteinuria. Ultrasonographic findings included hyperechoic renal cortices, loss of corticomedullary junction definition, dilated pelves and irregularly shaped small kidneys. Renal histopathological findings included pericapsular and interstitial fibrosis, inflammatory cell infiltration, dilated tubules, sclerotic glomeruli and dystrophic calcification. Survival time of the dogs varied from zero to over five years after diagnosis. CLINICAL SIGNIFICANCE: This paper documents features of the presentation and progression of juvenile nephropathy in boxer dogs. While juvenile nephropathy has been reported in individual cases of boxer dogs previously, this is the first reported case series.     

Amyloidosis in the black-footed ferret (Mustela nigripes).

This study describes clinical, histologic, immunohistochemical and electron microscopic features of amyloid A amyloidosis occurring in black-footed ferrets (Mustela nigripes) from eight U.S. zoological institutions. Ferrets had nonregenerative anemia, serum chemistries consistent with chronic renal disease, and proteinuria. Amyloid was present in a variety of tissues, but it was most severe in renal glomeruli and associated with tubular protein loss and emaciation. Congo red/potassium permanganate (KMnO4) and immunohistochemical stains revealed that the amyloid was of the AA type. Concurrent diseases and genetic predisposition were considered the most important contributing factors to development of amyloidosis. Analysis of the genetic tree did not reveal convincing evidence of a common ancestor in the affected ferrets, but a genetic predisposition is likely because all the captive black-footed ferrets are related.     

Acute encephalitis and hydrocephalus in dogs caused by canine parainfluenza virus

Gnotobiotic puppies were inoculated intracerebrally with a strain of canine parainfluenza virus (CPI-78-238). Four of eight dogs developed histological evidence of acute encephalitis. Clinical signs of encephalitis were seen in two of these four dogs; one had signs and lesions of interstitial pneumonia. Of six inoculated dogs observed for six months after infection, five developed internal hydrocephalus. Virus was reisolated from two dogs with acute encephalitis but not from dogs with hydrocephalus. Hemagglutination-inhibition antibodies persisted throughout the observation period of six months at high levels in the serum and cerebrospinal fluid of hydrocephalic dogs.     

Clinical, radiological and pathological features of 12 Irish setters with canine leucocyte adhesion deficiency

The clinical, radiological and pathological findings in 12 dogs with canine leucocyte adhesion deficiency (CLAD) from six litters are described. All the dogs were younger than 15 weeks at admission, all had been febrile and 11 had been treated with antibiotics. Seven had been treated for omphalophlebitis. At admission, all had gingivitis, lymph node enlargement and profound neutrophilia. Ten dogs were radiographed and showed various skeletal lesions compatible with metaphyseal osteopathy, craniomandibular osteopathy and osteomyelitis. Four dogs had clinical signs of respiratory distress and seven exhibited a mild interstitial pneumonia at necropsy. Six dogs had skin wounds, with strikingly few neutrophils seen on stained sections. All dogs were euthanased before six months of age due to severe and incurable infections. The clinical signs, radiological features and haematology were strongly suggestive of CLAD. The diagnosis was confirmed by granulocyte function tests and flow cytometry, which revealed impaired adhesion, impaired C3b-mediated phagocytosis and absence of adhesion proteins CD11b/CD18.     

Anosmia associated with canine distemper

The sense of smell in dogs infected with canine distemper virus (CDV) was examined by use of EEG olfactometry, behavioral olfactometry, and electro-olfactography. Infection with CDV was confirmed by a direct immunofluorescence technique in 8 active cases and was suggested by clinical history compatible with canine distemper 10 to 26 weeks earlier in 6 cases. Pathologic alterations of the olfactory mucosa in 3 clinically affected dogs was examined by light microscopy. Infection with CDV was found to be associated with anosmia and lack of recorded responses on electro-olfactogram in 8 of 8 dogs with clinical signs of acute distemper from naturally acquired infections. Anosmia was found in 5 of 6 dogs that had recovered from acute distemper 10 to 26 weeks earlier. The sixth dog had hyposmia, with abnormalities on the electro-olfactogram. Histologic examination was not performed on the 6 dogs that had recovered. Histologic lesions observed at necropsy in 3 dogs that had had clinical signs of acute distemper were those of subacute purulent rhinitis and atrophy of the olfactory epithelium. Altered olfactory function could be explained by mucopurulent exudate blocking odors from olfactory receptors in the acutely affected dogs, but alteration of olfactory function in the dogs that had recovered without clinical evidence of rhinitis could not be explained.     

Surgical treatment of adrenocortical tumors: 21 cases (1990-1996)

Twenty-four adrenocortical tumors were surgically removed from 21 dogs. Histopathological examination confirmed 18 carcinomas and six adenomas. Four dogs died in the perioperative period. Fifteen of the 17 dogs that survived the perioperative period had long-term resolution of their clinical signs. Two dogs with incompletely resected tumors were treated with mitotane to control their clinical signs. Overall median Kaplan-Meier life-table survival for dogs with carcinomas was 778 days (range, one to 1,593 days). Median survival for dogs with adenomas was not reached (range, 11 to 730 days). Histopathological diagnosis, histopathological cellular features, age of the dog, and tumor size were not prognostic of outcome.     

Hyperadrenocorticism in 10 dogs with skin lesions as the only presenting clinical signs

Ten dogs that had skin lesions as the only presenting signs of hyperadrenocorticism (HAC) and as the owners' primary complaint are described. Dogs were included if the initial examination was for skin disease, there were no signs of systemic illness on initial presentation and there was a confirmed diagnosis of HAC by specific screening tests. Dogs were excluded if they had a severe disease that might interfere with screening tests for HAC or if the screening tests were not diagnostic. There were five males and five females; six dogs were intact. Nine dogs were diagnosed at ≥7 years. Eight dogs weighed ≤10 kg. Alopecia was present in nine dogs. Eight dogs had bacterial pyoderma, five had hyperpigmentation, and four had thin skin. One dog had unresolved dermatophytosis. Skin lesions resolved after treatment in eight dogs. One dog was not treated and one was lost to follow-up. This study showed that skin lesions may be the only clinical signs of HAC. The presence of the more common clinical signs of HAC, such as a non-pruritic, truncal alopecia and/or thin skin, without any systemic signs of HAC and/or the presence of poorly responsive skin infections warrant screening for this disease.     

Comparison of radiography and ultrasonography in the evaluation of renal lesions in the dog

Survey abdominal radiographs, excretory urograms, and nephrosonograms were obtained from 14 dogs with renal lesions. Renal enlargement was suspected on survey radiographs and confirmed by excretory urography in 13 dogs. Radiographic differentiation between a solid and cystic renal lesion was not possible in 9 dogs. Ultrasonography determined the presence of solid masses in 12 dogs, established the presence of a renal cyst in the opposite kidney in 1 dog, and revealed hydronephrosis in 2 dogs. Ultrasonography appeared to be more sensitive than radiography in differentiating the internal characteristics of renal lesions.     

Body cavity lipomas in six dogs

Histologically confirmed lipomas were surgically removed from the thoracic or abdominal cavities of six dogs. Three dogs had a large intra-abdominal mass causing severe abdominal distension. Two dogs had a mass extending into the pelvic canal, compressing the colon and causing obstipation. One dog with an intrathoracic mass had a history of coughing and intermittent cyanosis. All dogs had complete resolution of signs after surgical resection of the tumour. Recurrence occurred in one dog with an abdominal lipoma, two years after the initial surgery. This recurrent lipoma was treated successfully by surgical resection.